Download Heatstroke: Clinical Signs, Diagnosis, Treatment, and Prognosis

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Heatstroke: Clinical Signs, Diagnosis,
Treatment, and Prognosis
Carey Hemmelgarn, DVM
Kristi Gannon, DVM, DACVECC
Oradell Animal Hospital
Paramus, New Jersey
Abstract: Heatstroke is a complex disease process that, in its most severe form, can result in multiorgan dysfunction and death.
Heatstroke stems from the failure of the body’s thermoregulatory mechanisms, resulting in cellular damage and death. The organ
systems most commonly affected in this disease process include the gastrointestinal tract and the coagulation, renal, cardiac, pulmonary,
and central nervous systems. Heatstroke is diagnosed based on the patient history, physical examination, and clinicopathologic
findings. Treatment should be instituted immediately to improve patient outcome and includes active cooling, fluid resuscitation, and
supportive care. Patients with altered mental status, hypoglycemia, prolonged prothrombin time, and prolonged activated partial
thromboplastin time at admission have increased mortality rates. Additional negative prognostic indicators include elevated serum
creatinine level, delayed admission to the hospital, seizures, and obesity.
For more information, please see the companion article, “Heatstroke:
Thermoregulation, Pathophysiology, and Predisposing Factors.”
H
eatstroke is the most severe form of heat-related illness.
Recently, a new definition of heatstroke for human patients
has been proposed: “A form of hyperthermia associated
with a systemic inflammatory response leading to a syndrome of
multi-organ dysfunction in which encephalopathy predominates.”1
A similar disease process has been seen in veterinary patients.
Regardless of the definition, this disease process is often progressive
and can be life threatening.
Multiorgan dysfunction is the hallmark of heatstroke. Affected
organ systems often include the gastrointestinal tract and the
coagulation, renal, pulmonary, and central nervous systems.
Common sequelae of heatstroke include disseminated intravascular coagulation (DIC), acute lung injury or acute respiratory
distress syndrome, and acute kidney injury. This article discusses
the clinical signs and diagnosis of, as well as treatment options
and prognosis for, heatstroke.
Clinical Signs and Diagnosis
History and Patient Assessment
Patients suffering from heat-related illnesses have clinical signs that
vary greatly depending on the severity of the disease. Therefore, a
thorough history is key in the initial stages of heatstroke management. Often, the history includes exposure to increased environmental temperatures or strenuous exercise without acclimatization.
During the initial evaluation, owners should be questioned about
underlying medical conditions and concurrent medication administration. Known predisposing factors or heatstroke include obesity,
cardiovascular disease, neurologic/neuromuscular disease, upper
airway abnormalities, strenuous exercise, and confinement with
poor ventilation.
Patient assessment and treatment should be performed
simultaneously. Initial assessment of the patient using the CAB
(cardiovascular-airway-breathing) approach is essential for all
patients that are potentially suffering from a heat-related illness.
The patient should be assessed for the presence of a heartbeat, a
patent airway, and normal respiratory excursions. After the initial
assessment is done, a second, more comprehensive examination
of all body systems should be performed and appropriate therapies
initiated (FIGURE 1).
Evaluation of the patient’s cardiopulmonary systems to determine
if signs of shock are present should include a visual assessment in
conjunction with thoracic auscultation and assessment of perfusion
parameters (mentation, pulse quality, mucous membrane color,
capillary refill time; TABLE 1).
Apnea or agonal breathing is an indication for immediate intubation to secure the patient’s airway. Breathing patients should
be examined closely for evidence of upper airway obstruction
(inspiratory stridor), abnormal respiratory patterns, or both, as
upper and lower airway disease can be concurrent in patients with
heatstroke. Systematic auscultation of the thoracic cavity aids in
identifying cardiac arrhythmias, murmurs, and adventitious breath
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Heatstroke: Clinical Signs, Diagnosis, Treatment, and Prognosis
the patient’s status. In patients with neurologic
abnormalities, a modified Glasgow Coma Scale is
Mucous
recommended to facilitate serial neurologic exams.3
Membrane Color Capillary Refill Time
Pulse Quality
Stage of Shock
The rectal temperature of patients with heatstroke
can indicate hypothermia, normothermia,
Normal
Normal or prolonged
Normal to hyperdynamic Compensatory
or hyperthermia.4 It is important to remember
Pale
Prolonged
Fair to poor
Decompensatory
that patients that are affected severely by heatrelated illnesses may have a normal or subnormal
Hyperemic
Fast to normal
Variable
Decompensatory
presenting temperature. This may be caused by
previous treatments by owners or referring vetsounds, further directing treatment and diagnostic recommenerinarians or by the presence of varying stages of shock.
dations. Most heatstroke patients are tachycardic and tachypneic,
Hydration should be assessed to guide fluid therapy planning.
but heart and respiratory rates vary depending on the presence and
Evaluation of the patient’s mucous membranes (dry versus moist)
stage of shock. Potential cardiac arrhythmias should be evaluated
and skin turgor can help determine the degree of dehydration.
further by electrocardiography; based on a 2006 retrospective
Mucous membranes and unhaired skin should be examined for
study,2 up to 25% of patients presenting with heatstroke have
evidence of hemorrhage (petechiae or ecchymoses) because of
confirmed arrhythmias.
the risk of developing coagulopathies or DIC caused by direct
A focused neurologic examination should be performed at
thermal cytotoxicity. A rectal exam should be performed to evalinitial presentation and include the evaluation of patient mental
uate for evidence of overt gastrointestinal hemorrhage, mucosal
status, behavior, and cranial nerves. Mental status can range from
sloughing, or melena.5 Abdominal palpation can help identify
normal to obtunded or comatose. Heatstroke patients can also
underlying medical conditions through detection of intraabpresent with ongoing seizure activity or in a postictal state. In a
dominal neoplasia, organomegaly, ascites (palpable fluid wave),
recent retrospective study of canine heatstroke patients, neurologic
or pain. These findings can help guide diagnosis and treatment
abnormalities were common; 35% of patients presented with seizure
recommendations.
activity at or before presentation. Of this population, 47% had an
obtunded mental status and 24% presented in a comatose state.2
Diagnostics
The presence of seizure activity, altered mental status, or both is
Blood should be collected during the initial assessment and can
associated with an increased risk for death in canine heatstroke
be drawn from an IV catheter during placement to provide baseline
patients. A complete neurologic assessment, including gait (if
values for parameters to be monitored throughout treatment.
ambulating), postural reactions, and
spinal reflexes,
should beclinicalImmediate
point-of-care
tests,
Hemmelgarn
et al. Heatstroke:
signs, diagnosis,
treatment,
and including
prognosis. packed cell volume/total
Contin Pract
Vetcan
2013;35(5).
performed once the patient is stable. Compend
Serial neurologic
exams
be
solids, blood glucose, electrolytes, blood gases, lactate, and kidney
used to monitor the response to treatment and detect deterioration in
values (blood urea nitrogen/creatinine) can be used to guide the
Table 1: Perfusion Parameters and Potential Stages of Shock4
Initial assessment
Cardiovascular
Airway
Heartbeat
No
Initiate CPR
Yes, continue with
assessment
Perfusion
Yes
Hypovolemia
Regular rhythm
Crystalloid fluids
Patent
Normal perfusion
Continue
monitoring
Breathing
Not patent
Intubation
Spontaneous
Continue
monitoring
Absent or agonal
Intubation
Maintenance fluid
therapy
No, recommend
electrocardiogram
Figure 1. Algorithm for initial patient assessment.
Figure 1. Algorithm for initial patient assessment.
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Heatstroke: Clinical Signs, Diagnosis, Treatment, and Prognosis
initial therapeutic plan. A complete database should also be performed, including a complete blood count (CBC), serum chemistry
panel, urinalysis, and coagulation testing.
Common abnormalities on the CBC include leukocytosis or
leukopenia, anemia, hemoconcentration/polycythemia, the presence
of nucleated red blood cells (nRBC), and thrombocytopenia.
Leukocytosis could indicate an acute inflammatory response
from the episode of heat stress, a response to infection, or an underlying bone marrow disease. Leukopenia can be seen secondary to
sepsis or bone marrow disease. Anemia could indicate acute blood
loss from hemorrhage or anemia of chronic disease associated
with a preexisting medical condition. A blood smear should also
be evaluated for the presence of nRBC. In a 2009 retrospective
study, 90% of dogs with heatstroke had nRBC noted on a blood
smear.6 This finding is unique to dogs and has not been noted with
human heatstroke patients. The presence of nRBC was speculated
to be caused by direct thermal cytotoxicity to the patient’s bone
marrow.6 Thrombocytopenia was seen in 83% of canine heatstroke patients in a 2006 retrospective study.2 The authors of this
paper proposed the following causes for thrombocytopenia in
the study’s population: secondary platelet consumption caused by
vasculitis, gastrointestinal bleeding, and hyperthermia-induced
platelet aggregation.2
Chemistry panel abnormalities can include elevations of alanine
aminotransferase, total bilirubin, blood urea nitrogen, creatinine,
creatine kinase, and glucose levels. Canine patients with heatstroke commonly have elevations in alanine aminotransferase
and bilirubin levels caused by direct hepatocellular hypoxia.4,5
Elevations of blood urea nitrogen and creatinine levels can be
prerenal as a result of dehydration, renal as a result of direct cytotoxicity and ischemic insults, or both. Rising creatinine levels
during fluid therapy have been linked with increased mortality in
canine heatstroke patients.4 Creatine kinase elevation is expected
as a result of diffuse muscle damage (rhabdomyolysis).4 Alterations in
the patient’s blood glucose can be multifactorial. Hypoglycemia
can be secondary to sepsis from gastrointestinal bacterial translocation, hepatocellular injury, prolonged seizure activity, or an
unrelated preexisting condition (e.g., insulinoma).4,5 Persistent
hypoglycemia despite treatment was associated with increased
mortality in canine heatstroke patients.4,7
Acid-base and electrolyte abnormalities can include metabolic
acidosis with compensatory respiratory alkalosis5 and alterations
in sodium, potassium, phosphorus, and calcium. Metabolic acidosis
can be caused by global hypoxia that can lead to lactic acid production from anaerobic metabolism, or by uremic acids in patients
with impaired renal function.8 A patient’s sodium level can be can
be highly variable with heatstroke. Hypernatremia can be caused
by pure water loss and dehydration, while hyponatremia can be
caused by increased hypertonic fluid loss (e.g., vomiting, diarrhea).8,9
Hyperkalemia can be seen as a result of cellular death, particularly
with rhabdomyolysis.10 Hypophosphatemia and hypocalcemia
may be seen; however, the underlying mechanism is unknown.8,11
A urinalysis should be completed to evaluate the patient’s
urine concentrating ability and to detect the presence of myoglobin,
bilirubin, or casts within the urine. Confirming a normal to elevated
urine specific gravity at admission can serve as a baseline for
evaluation of the patient’s hydration status and current renal
function. Isosthenuria at admission may indicate a preexisting or
secondary kidney injury.
Coagulation testing should be pursued in all heatstroke patients,
especially those with suspected active blood loss (hematochezia,
hematemesis, petechiae/ecchymoses, anemia with hypoproteinemia). Baseline coagulation testing includes a partial thromboplastin
time, prothrombin time, and platelet count. If platelet dysfunction
is suspected, a buccal mucosal bleeding time should be performed.
If available, a thromboelastogram is useful in evaluating all aspects
of coagulation and identifying both hypo- and hypercoagulable
patients. As mentioned earlier, heatstroke patients are at risk for
development of DIC. Early and serial evaluations of a peripheral
blood smear are recommended. The presence of schistocytes
may support a diagnosis of DIC.5 Additional hematologic changes
commonly associated with DIC that may help to confirm the
diagnosis include thrombocytopenia, prolonged prothrombin
time, prolonged activated partial thromboplastin time, hypo- or
hyperfibrinogenemia, low antithrombin levels, and the presence
of fibrin degeneration products or D-dimers.12
Thoracic radiography should be performed for any patient
with cardiopulmonary dysfunction, such as abnormal lung auscultation (adventitious breath sounds), persistent hypoxemia,
irregular breathing patterns, heart murmur, or cardiac arrhythmia.
Patients with respiratory compromise can benefit from serial pulse
oximetry readings, blood gas analyses, or both to identify and
characterize underlying hypoxemia and assess response to oxygen
therapy. Additional advanced diagnostic testing (e.g., abdominal/
thoracic ultrasonography, magnetic resonance imaging) should
be considered in geriatric patients or those presenting with nonexertional heatstroke without a known predisposing factor(s).
Treatment
Treatment should begin as soon as possible to increase the chance
of survival and should be prioritized to address the most critical
clinical abnormalities identified on the primary survey (TABLE 2).
Treatment Options for Owners at Home
Owners who contact a hospital with a patient with possible heatstroke should be encouraged to actively cool the patient while en
route to the hospital. At-home cooling should not delay arrival to
the hospital but rather be performed simultaneously. Active
cooling can be accomplished by applying cool water to the patient,
either with a hose or other water source or with presoaked towels
placed over the patient. This assists in heat dissipation through
evaporation and convection when used in conjunction with
open windows or air conditioning while driving to the hospital.8
If this cannot be accomplished safely, it should be avoided and the
patient should be brought to the hospital immediately. Patients
should not be submerged in a cold-water bath due to the risk
of drowning if neurologically impaired; in addition, extreme
peripheral vasoconstriction may impair heat dissipation.
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Heatstroke: Clinical Signs, Diagnosis, Treatment, and Prognosis
Hospital-initiated Treatment
Patients that are obtunded or comatose at presentation should be
intubated immediately and their airway secured. Supplemental
oxygen and intermittent positive-pressure ventilation should be
administered until spontaneous breathing is deemed adequate.
Initial treatment should be targeted at reducing ongoing hyperthermia and correcting cardiovascular collapse to minimize further
organ injury.
Active Cooling
Active cooling is an essential part of treatment for heatstroke patients
and is achieved by maximizing heat dissipation mechanisms.
Cooling techniques should be instituted, including applying cool
water to the patient while increasing air circulation over the body
with fans to improve evaporation. Care should be taken in soaking
patients with thick haircoats because wet hair can act as an insulation
barrier and limit heat dissipation. Thinly haired areas (ventral
abdomen, axilla, and inguinal regions) should be cooled by applying
towels soaked with cool water. Ice packs should be avoided to
prevent cutaneous vasoconstriction that may cause shunting of
heated blood to central visceral organs.5 Massaging extremities is
a technique used in human medicine to improve peripheral circulation during active cooling.13 Active cooling should be stopped
when the patient’s temperature is 39.5 °C (103.1°F) because cooling
will continue and there is a risk of progression to hypothermia. A
2007 study reported that cold-water immersion in human patients
with exertional heatstroke improved morbidity and mortality but
may be detrimental in cooling patients with nonexertional heatstroke.14 Immersion is not currently recommended in veterinary
patients due to the high prevalence of nonexertional heatstroke.
Otherwise, no means has proven superior to immersion in reducing
core body temperature while reducing mortality/morbidity in
human heatstroke patients.15
Cold-water enemas and gastric lavage have been suggested in
literature. These techniques have been associated with adverse
outcomes; gastric lavage is associated with an increased risk of
aspiration pneumonia, and both techniques may further gastrointestinal permeability. Therefore, these techniques cannot be
recommended at this time. Peritoneal lavage has been investigated
in animal studies with mild increase in survival versus control
groups but is not currently recommended in human medicine.15,16
Pharmacologic agents to hasten cooling or reduce core temperature
(e.g., NSAIDs, dantrolene) have not been proven beneficial and
are discouraged because of potential negative effects on organ
function (e.g., acute kidney injury, gastric ulceration).9,17 Other
novel and experimental methods of active cooling for human
exertional heatstroke patients have included noninvasive external
cooling systems, hyperbaric oxygen therapy, and endovascular
cooling devices, but they have yet to be validated in veterinary
patients.18–20
Cardiovascular Support
Heatstroke is characterized by a state of distributive shock with
absolute or relative volume deficit. As a result, fluid resuscitation
should be instituted during
Key Facts
the process of active cooling.
Restoring the patient’s cir• Heatstroke, the most severe form of
culating volume improves
heat-related illness, is characterized
cutaneous vasodilation and
by a core temperature >104°F
perfusion of visceral organs.
(>40°C) and central nervous system
The initial goal of fluid
abnormalities.
therapy is to quickly restore
perfusion. Balanced elec• Patients with altered mental status
trolyte crystalloid fluids are
have increased mortality rates
recommended as the initial
compared with those with
fluid choice. Fluids should
non-altered mental status.
be administered as incre• Patients can be severely affected
mental boluses (e.g., 10 to
by heat-related illnesses but have
20 mL/kg over 10 to 15 min)
a normal or subnormal presenting
with subsequent patient retemperature.
assessment to guide further
administration. Supplemen• Early initiation of active cooling
tation with synthetic colloid
by owners during transport to the
boluses should be considhospital may reduce the risk of
ered in hypoproteinemic
death from heatstroke.
patients or those refractory
to large-volume crystalloid
administration. Excessive crystalloid therapy may lead to dilutional
coagulopathy and worsen already low colloid osmotic pressure
in hypoalbuminemic patients.
If hypotension persists despite adequate fluid therapy, vasoactive
agents (dopamine, vasopressin, norepinephrine, dobutamine) should
be considered, as distributive shock secondary to bacterial sepsis
is common. End points of resuscitation should include improved
mentation with normalization of heart rate, respiratory rate, temperature, blood pressure, and hyperlactatemia, if measured. Once the
patient is hemodynamically stable, its hydration status should be
assessed and a fluid plan instituted to replace any ongoing deficits.
Glucose supplementation may be required either on presentation
or later during hospitalization in response to hypoglycemia. Blood
glucose levels should be checked frequently and supplemented
using 50% dextrose as an initial bolus followed by a continuous
infusion if hypoglycemia persists. Acid-base and electrolyte
abnormalities are pervasive in patients with heatstroke and dynamic
throughout the course of treatment. Most abnormalities do not
resolve immediately; therefore, monitoring of changes and trends
is recommended to guide treatment adjustments.
Antibiotics should be instituted in patients with signs of sepsis
as well as patients with hypoperfusion and evidence of gastrointestinal mucosal disruption (hematochezia, hematemesis, melena,
or prolonged anorexia) because of the increased risk of bacterial
translocation. Broad-spectrum bactericidal antibiotic coverage that
is effective against gram-negative, gram-positive, and anaerobic
bacteria is recommended.9 Coverage should be continued until
the patient’s cardiovascular status is stable, enteral intake is good,
and gastrointestinal signs are resolving.
Based on the patient’s red blood cell count, platelet count, and
coagulation testing results, the use of blood products may be
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Heatstroke: Clinical Signs, Diagnosis, Treatment, and Prognosis
Table 2. Pharmacologic Treatment Recommendations12,26
Category of Medication
Indication
Drug
Dose
IV fluids (crystalloid)
Hypovolemia
Lactated Ringer solution
10 mL/kg bolus (can be repeated, being cautious if
exceeding patient’s blood volume)
Normosol-R
Plasmalyte 148
IV fluids (crystalloid)
Hydration
Lactated Ringer solution
Patient weight <2 or >50 kg: (BWkg0.75)70 mL/day
Normosol-R
Patient weight 3–49 kg: (BWkg × 30) + 70 mL/day
Plasmalyte 148
IV fluids (colloid)
Antibiotics
Hypotension
Hetastarch 450/0.7
Hypovolemia
Vetstarch 6% 130/0.4
Bacterial infection
Ampicillin
22 mg/kg q8h
Enrofloxacin
5–10 mg/kg q24h
Cefazolin
22 mg/kg q8h
Plasma
Coagulopathy
Osmotic agents
Cerebral hypertension
Gastrointestinal protectants
Mucosal injury
5 mL/kg bolus (can be repeated, being cautious if exceeding
20 mL/kg/d)
10 mL/kg
Hypertonic saline
3–5 mL/kg bolus
Mannitol
1 g/kg over 30 minutes
Famotidine
0.5–1 mg/kg q24h
Cimetidine
5–10 mg/kg q8h
Sucralfate
0.25–1 g q8h
Sodium channel inhibitor
Ventricular arrhythmias
Lidocaine
2 mg/kg IV bolus (dogs)
Vasopressors
Hypotension
Dopamine
3–10 µg/kg/min IV
Vasopressin
0.5–4 mU/kg/min IV
Norepinephrine
0.05–2 µg/kg/min IV
Dobutamine
2–20 µg/kg/min IV (dogs)
1–5 µg/kg/min IV (cats)
Dextrose
Electrolyte supplementation
Hypoglycemia
Hypokalemia
50% Dextrose
0.5 mL/kg diluted 1:1 as a bolus and supplementation
added to crystalloid fluids
25% Dextrose
1 mL/kg diluted 1:1 as a bolus and supplementation added
to crystalloid fluids
Potassium chloride
Supplementation is based on the patient’s potassium level
but should not exceed 0.5 mEq/kg/hr IV
indicated. The product required is based on the patient’s underlying
needs. Coagulopathic patients may benefit from fresh frozen plasma,
whole blood, or platelet-rich plasma transfusions. Anemic patients
should be monitored closely and evaluated on an individual basis
to determine if a transfusion is indicated. Indications for transfusions
should be based on the patient’s hematocrit (<25%) in conjunction
with abnormal perfusion parameters. Anemic patients benefit
most from packed red blood cell or whole blood transfusions. A
complete discussion of transfusion medicine is beyond the scope
of this paper, but there are established resources regarding transfusion medicine.21
Frequent reassessment of patient cardiopulmonary status
should include monitoring of blood pressure, heart rate, respiratory
rate and effort, thoracic auscultation, and perfusion parameters.
Cardiac arrhythmias can be present at the time of admission or
develop during hospitalization and should be identified and
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Heatstroke: Clinical Signs, Diagnosis, Treatment, and Prognosis
characterized immediately. Continuous ECG monitoring should
be instituted if frequent and persistent arrhythmias are noted. Before
initiating antiarrhythmic medication, underlying hypovolemia,
pain, anxiety, acid-base disturbances, and electrolyte abnormalities
should be ruled out or appropriately treated. Thoracic radiography,
pulse oximetry, and arterial blood gas analysis are useful in identifying and addressing changes in pulmonary status. Supplemental
oxygen is indicated in any patient with pulmonary dysfunction.
Placement of an indwelling urinary catheter is indicated in
heatstroke patients with suspected kidney injury. This allows
quantitative measurement of urine output to tailor ongoing fluid
therapy and assessment of urine quality (hematuria, myoglobinuria,
casts). Early identification of oliguria or anuria can improve outcome
through judicious use of IV fluids in order to avoid overhydration.
Maintaining a sterile, closed system is essential to reduce the risk
of nosocomial infections. Indwelling urinary catheters should be
limited to patients that are at risk of oliguria or anuric renal failure.
Universal placement of urinary catheters in all heatstroke patients
could place these patients at undue risk of ascending urinary
tract infection.
Gastrointestinal support should be provided due to the increased
prevalence of mucosal injury. Antiemetic therapy may be warranted
based on patient history and clinical signs. Proton pump inhibitors
or H2 blockers should be considered to decrease the risk of stressrelated mucosal disease.22 Sucralfate is indicated if gastric ulceration
is suspected but is ineffective in preventing gastric ulcers. Administration of oral medications should be reserved for patients that
have an intact swallow reflex. Nutritional support is essential to
restoring gastrointestinal integrity and should be instituted as
soon as possible, but only after the patient’s cardiovascular status
is stable. This is best accomplished through enteral feeding. If the
patient cannot tolerate enteral feeding or is neurologically compromised (i.e., comatose or absent swallow reflex), parenteral
nutrition is indicated.
For patients with signs of central nervous system dysfunction,
serial neurologic evaluations in conjunction with blood pressure
monitoring should be used. If intracranial hypertension is suspected
and the patient is adequately hydrated, 7.5% hypertonic saline may
be superior to mannitol because it reduces the risk of dehydration
caused by osmotic diuresis.23
Corticosteroid use is controversial in heatstroke patients;
careful risk evaluation is needed before proceeding with administration. Although some benefits have been found with steroid
therapy in experimental models, risks are also present, including
gastrointestinal ulceration and immunosuppression. Routine use
of corticosteroids is discouraged. Use of these agents should be
decided on a case-by-case basis to confirm that the benefits of
administration outweigh the risks.
Prognosis
Heatstroke patients have many variables that make it difficult to
predict outcome. Published mortality rates range from 50% to
56% in canine heatstroke studies.2,6 Negative prognostic indicators
at hospital admission that have been identified in veterinary patients
include altered mental status, hypoglycemia, prolonged prothrombin
time (>18 seconds), and prolonged activated partial thromboplastin time (>30 seconds).2,6 Other reported negative prognostic
indicators include elevated serum creatinine level (>1.5 mg/dL),
delayed admission to the hospital (>90 minutes), seizure activity,
and obesity.2 Based on our clinical experience, a patient’s response
to aggressive therapy in the first 12 to 24 hours is likely a better
determinant of true outcome. In human heatstroke patients, high
levels of high mobility group box-1 (HMGB1) protein were noted
to peak at 6 hours and correlated with a negative prognosis.24
HMGB1 is a new topic of research in a variety of inflammatory
conditions in canine patients and an area of further research for
veterinary patients.25
Summary
Heatstroke is common in human and veterinary medicine. The
body is equipped with intricate mechanisms for thermoregulation,
but with prolonged exposure or extreme hyperthermia, these
mechanisms eventually fail. Clinical signs vary depending on the
severity of the disease, presence of predisposing factors, and underlying disease processes. Early diagnosis of heatstroke in conjunction
with rapid initiation of treatment is key to improving patient outcome. Treatment is centered on active cooling, restoration of patient
volume status, and prevention of multiorgan failure. Therapies
can be multifaceted and must be tailored to the patient. Outcome
depends largely on response to treatment.
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Heatstroke: Clinical Signs, Diagnosis, Treatment, and Prognosis
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3 CE Credits
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1. Which neurologic abnormality(ies) at presentation are
associated with increased mortality?
6. The presence of schistocytes may be an early indicator of
which sequela of heatstroke?
a. tetraparesis
a. acute renal failure
b. presence of seizure activity
b. acute respiratory distress syndrome
c. altered mental status
c. acute liver failure
d. b and c
d. disseminated intravascular coagulation
2. Which perfusion parameters should be assessed during the
initial examination?
7. Active cooling should be discontinued at what core body
temperature?
a. capillary refill time
a. 101.5°F (38.6°C)
b. mucous membrane color
b. 103.1°F (39.5°C)
c. pulse quality
d. all of the above
3. Leukocytosis is suspected to develop in heatstroke patients
because of (an)
a. acute inflammatory response.
b. dehydration.
c. response to infection.
d. a and c
4. The presence of nucleated red blood cells in heatstroke
patients is speculated to be caused by
a. direct thermal cytotoxicity to red blood cells.
b. chronic anemia.
c. direct thermal cytotoxicity to the bone marrow.
d. none of the above
5. The first treatment step to restoring perfusion in heatstroke
patients is administration of
c. 103.8°F (39.9°C)
d. 104.5°F (40.3°C)
8. Air conditioning and open windows while driving to the
hospital are two ways to increase heat dissipation through
what mechanism(s)?
a. conduction
b. convection and evaporation
c. radiation
d. none of the above
9. Which is of the following is not a poor prognostic indicator?
a. persistent hypoglycemia
b. persistent increased creatinine
c. decreased prothrombin time
d. altered mental status
10. Patients that are adequately hydrated and are suspected
of having increased intracranial pressure should be
treated with
a. gastrointestinal protectants
a. antibiotics.
b. antibiotics
b. hypertonic saline.
c. fresh frozen plasma
c. mannitol.
d. fluid therapy (crystalloid and colloid).
d. valium.
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